Indeed, several possible mechanisms sustain the association between AF and (ED), including the impaired rheology after AF-induced turbulent flow, the reduced production of nitric oxide (NO) in the left atrium, the unbalanced release of endothelin-1 (ET-1), and the activation of systemic factors, such as the renin-angiotensin aldosterone system (RAAS) and inflammatory signaling that may sustain and promote ED progression. This evidence concerns the gene REN and atrial fibrillation.